Periodontal Inflammation: the Oral-Body Health Connection a Peer-Reviewed Publication Written by Richard Nejat, DDS; Daniel Nejat, DMD, Morris Nejat, MD

Earn 2 CE credits This course was written for dentists, dental hygienists, and assistants.

Periodontal Inflammation: The Oral-Body Health Connection A Peer-Reviewed Publication Written by Richard Nejat, DDS; Daniel Nejat, DMD, Morris Nejat, MD

PennWell designates this activity for 2 Continuing Educational Credits Publication date: September 2007 Go Green, Go Online to take your course Review date: March 2011 Expiry date: February 2014 This course has been made possible through an unrestricted educational grant. The cost of this CE course is $49.00 for 2 CE credits. Cancellation/Refund Policy: Any participant who is not 100% satisfied with this course can request a full refund by contacting PennWell in writing. Educational Objectives redness due to open blood vessels, heat due to warmth of Upon completion of this course, the clinician will be able blood, swelling due to edema, pain due to stimulation of to do the following: pain receptors, and loss of function due to edema.1 1. List and describe the mechanism by which periodontal Periodontitis is the inflammation of the periodontium disease causes production of inflammatory mediators (gingiva and underlying connective tissue) resulting in that enter the systemic circulation and affect organ features such as clinical attachment loss, alveolar bone systems in the body loss, and periodontal pocketing. In periodontitis, one can 2. List and describe the mechanism by which inflamma- see enlargement or recession of the gingivae, bleeding tory mediators effect vessel plaque formation and lead upon probing, increased tooth mobility, drifting of teeth, to an increased risk of cardiovascular disease and/or tooth exfoliation. Chronic periodontitis is a slowly 3. List and describe the mechanism by which periodontal progressing disease process that may occur continuously disease mediators worsen the condition in diabetes mellitus or in bursts of activity. Histologically, the gingival tissue 4. Describe the association of periodontal disease and from chronic periodontitis displays junctional epithelium the increased risk of development of pneumonia and more apical to the cemento-enamel junction, loss of col- COPD in the elderly lagen fibers subjacent to the pocket epithelium, bone loss, 5. Describe the probable association of periodontal numerous neutrophils (polymorphonuclear cells (PMNs), disease, tooth loss, and osteoporosis and dense inflammatory cell infiltrate with plasma cells, 6. Describe how appropriate treatment of periodontal lymphocytes, and macrophages.2 disease can lead to improvement in outcomes in many Tissue damage in chronic periodontitis is the result of of the above disease processes. major inflammatory and immunopathologic components activated by the host response. These include alteration of Abstract fibroblast function, activation of macrophages to release Inflammation represents the body’s protective response collagenase and other lytic enzymes, activation of lympho- to injury and tissue destruction. Its purpose is to destroy, cytes, modulation of fibroblast growth, collagen synthesis, dilute, or sequester the injurious agent and the injured and stimulation of bone resorption. Prostaglandins and tissues in order to permit healing. Inflammation can also cytokines appear to be critically involved in tissue destruc- be potentially harmful. Clinical signs of inflammation tion caused by periodontitis.2 are redness due to open blood vessels, heat due to warmth Concepts of the etiology of periodontitis imply a of blood, swelling due to edema, pain due to stimulation bacterial infection as the primary cause of the disease. of pain receptors, and loss of function due to edema. Peri- Gingival inflammation is the result of plaque, or bacterial odontitis is the result of inflammation to the periodon- biofilm, which contains gram negative bacteria such as P. tium, and cytokines, or chemical mediators, are the result gingivalis, B. forsythus, and P. intermedia, amongst many of infl ammatory cells fighting against bacterial plaque. others.2 These bacteria possess complex carbohydrates and High amounts of these mediators can affect the body’s proteins on their cell wall, called endotoxins or lipopoly- systems, especially the arteries and can potentially cause saccharides (LPSs). When these molecules are detected by more harm in a patient with compromised cardiovascular the host, a protective response ensues, resulting in inflam- health. Dental professionals should assess risk for pa- mation, recruitment of white blood cells (WBCs), and tients with diagnosed (or undiagnosed) diseases such as release of cytokines and chemical mediators. The chemical diabetes, respiratory diseases, and osteoporosis and refer mediators that cause the main systemic problems are IL- patients to a physician or periodontist as necessary. It is 1, IL-6, and tumor necrosis factor-alpha (TNF-α). The very important to evaluate and monitor oral hygiene in function of IL-1 is to recruit osteoclasts (bone-resorbing at risk patients. The inclusion of antimicrobials as a part cells), which remove bone matrix. The function of IL-6 is of patient home care to enhance plaque control should to increase fibrinogen, which helps in the clotting mecha- be considered. nism of injured blood vessels. The function of TNF-α is to primarily increase C-reactive proteins (CRPs) which Introduction recruit more macrophages to the site of injury. These me- Inflammation represents the body’s protective response diators, although helpful in fighting insult to the body, can to injury and tissue destruction. This response consists of be harmful as well. a spectrum of highly coordinated events that occur at the cellular and tissue level. Its purpose is to destroy, dilute, Periodontitis and Cardiovascular Disease or sequester the injurious agent and the injured tissues Atherosclerosis is the thickening and hardening of arteries in order to permit healing. Inflammation is a defensive due to plaque buildup on arterial walls. This is a chronic mechanism intended to protect the host, but can also be inflammatory condition that affects injured arteries. There potentially harmful. Clinical signs of inflammation are is growing evidence that infectious agents are causing this

2 www.ineedce.com injury, thereby resulting in this chronic inflammation. This To see if arteries are inflamed as a result of atherosclerosis, chronic inflammatory response increases the circulation a physician can test for CRPs by using a simple blood test at of mediators such as C-reactive proteins and fibrinogen. the same time the patient is being checked for cholesterol. There is a link between inflammation and atherosclerosis, The risk for CVD can be determined from the results. and it suggests that chronic infections, such as chronic CRP Risk for CVD periodontitis, may predispose someone to cardiovascular Less than 1.0 mg/L Low disease or exacerbate some with existing cardiovascular 1.0–2.9 mg/L Intermediate disease (CVD). The following is suggested regarding in- Greater than 3.0 mg/L High flammatory mediators common in chronic periodontitis and CVD:3 • C-reactive proteins: found in chronic periodontitis Monitor your patients’ blood pressure at initial exams and on and increased levels in the blood will cause damage to a yearly basis, as they may have undiagnosed or uncontrolled hypertension. If medications are listed, ask if they adhere to the smooth muscles of blood vessels and collection of dosing recommendations. macrophages. • IL-1: found in association with increased risk of severe Normal <120/<80 periodontitis and inside atherosclerotic plaques. Mild Hypertension 120–140/80–90 • TNF-α: also found in chronic periodontal infections. Systemically, it increases the synthesis of triglycerides Hypertension >140/>90 from the liver. An elevated triglyceride level is associated with lowered “good lipids,” known as HDL (high-density lipoproteins). This is associated with Healthy Heart Habits* CHD (coronary heart disease). • Fibrinogen: synthesized by the liver due to elevation • Eat a heart-smart diet including a variety of fruits, vegetables, and grains. of IL-6. IL-6 is also very high in chronic periodonti- • Exercise regularly. tis. Fibrinogen is a clotting factor that is common in • Limit soda, candy, alcohol, and sodium. creating thrombi (clots) in the blood vessels resulting • Identify and reduce sources of stress. in myocardial infarction (MI or “heart attack”) • Know your blood pressure. • Avoid smoking. and stroke.3 *American Heart Association Similarities in the pathogenesis of atherosclerosis and periodontitis have suggested a common underlying Clinical manifestations of cardiovascular disease biological mechanism for the two conditions. Most of the include hypertension (see above), fatigue after mild ac- evidence supporting a relationship between chronic peri- tivity or when lying down, ankle swelling, angina (chest odontitis and CVD is from studies performed in the late pains), myocardial infarction (heart attack), and cerebral 1980s and continued since then, associating patients with a vascular accident (stroke). It is essential that a thorough history of MI with poorer oral health than control subjects. medical history and blood pressure be taken during initial Those with acute MI had poorer oral health than those who oral examinations. If a patient answers affirmatively to were healthy.8 The incidence of mortality and coronary any of the above he/she may be taking medications, or, heart disease increased as the severity of periodontal dis- in fact, be unaware of his/her condition. If the patient ease increased.9 Patients with a 20% increase in periodontal is not well-controlled or if any question exists regarding bone loss had a 40% increase in developing chronic heart his/her health status, a medical consultation is essential. A disease (nonfatal MI, angina pectoris, and CHD deaths).4 well-controlled hypertensive patient, for example, will see P. gingivalis has the ability to induce the oxidization of his/her physician every three to six months. However, as “bad lipids,” known as LDL (low-density lipoproteins), a general dentist, it is essential to check the patient’s blood which are pathogenic for plaque formation on arterial pressure at initial examination and on a yearly basis.12 walls.5,6 CRP levels in patients with chronic periodontitis fall in the range of those who have cardiovascular disease.7 Chronic Periodontitis and Diabetes Mellitus Gentle mastication can induce the release of endotoxins Diabetes mellitus is one of the most common diseases from the mouth into the bloodstream, especially in patients in the United States. It is a chronic metabolic disorder with severe periodontitis. Also, periodontal pockets are a affecting carbohydrate, fat, and protein metabolism re- chronic source of passage of pro-inflammatory bacterial sulting in hyperglycemia. There are two types of diabetes components in the bloodstream.10 Periodontitis and gingi- mellitus: Type I is caused by defective secretion of insu- vitis are independently associated with the risk of cerebral lin, while type II is a result of impaired insulin action due ischemia (stroke).11 to tissue resistance. Appropriate measures can be taken to www.ineedce.com 3 control blood glucose levels and prevent both acute and • The increased inflammatory and cytokine response chronic complications.15 seen in diabetes is responsible for the dysregulation Patients with uncontrolled diabetes are prone to oral of lipid metabolism, insulin resistance, and long complications such as gingivitis, periodontal disease, fun- term microvascular complications. Chronic gal infections, and caries due to xerostomia. Uncontrolled periodontitis could magnify the already elevated diabetes also affects wound healing. However, those with cytokine response and contributes to the overall controlled diabetes will heal similarly to the nondiabetic burden of systemic inflammation. patient. The most common oral symptom of diabetes is the • Mechanical periodontal therapy with adjunctive increased prevalence and severity of periodontitis. Poorly- systemic doxycycline resulted in a 0.6% decrease in controlled diabetes results in rapid progression of gingivi- glycated hemoglobin.20 tis and periodontitis. The degree of metabolic control and duration of diabetes are closely associated with the severity Clinical manifestations of poorly-controlled or uncon- of periodontal disease.16 trolled diabetes are mostly polyphagia (increased hunger), polydipsia (increased thirst), polyurea (increased urina- Periodontal disease has two components: tion), pruritis (itching), weakness, increased susceptibility bacteria and host response. There is a bidirectional re- to infections, xerostomia leading to dental caries, burning lationship between periodontal disease and diabetes:17,18,19 mouth or tongue, altered taste sensation, candidiasis and • The presence of diabetes increases the prevalence, other opportunistic infections, and severe gingivitis and incidence, and severity of periodontitis.17,18 periodontitis. It should be a common practice to ask pa- • Advanced glycation end products (AGE), which tients if diabetes runs in the family. It is essential for the increase rapidly in poorly-controlled diabetics, tend dental clinician to look for these signs and consider refer- to transform important inflammatory cells into more ring the patient for a workup for diabetes.12 destructive cells, thereby resulting in more damage to many parts of the body as well as to the periodontium.18 • Hyperglycemia results in impaired neutrophil Look for clinical signs of uncontrolled or chemotaxis. Neutrophils are the first cells in the undiagnosed diabetes. Consider a physician host response against bacteria. Therefore, it can be referral when necessary. concluded that the host response will be impaired during gingivitis and periodontitis.17, 18, 19 • Diabetes leads to a two- to fourfold greater risk of The primary methods used for diagnosing diabetes severe bone loss. As glycemic control worsens, the mellitus are examining blood gluclose levels for short- or effects of periodontal disease become greater.17 long-term control via the glycated hemoglobin test, or • Due to the high vascularity of acute periodontitis, the HgbA1c test. This test is used because it monitors the inflamed periodontium may serve as an endocrine-like patient’s long-term control (a period of approximately source for TNF-α which antagonizes the effects of 90 days due to the fact that red blood cells are replaced insulin. Therefore, glycemic control can be improved every 90 days). Consequently, the patient needs to be with periodontal treatment in these patients.18 reassessed every three months for disease management. • Treatment of chronic periodontitis helps glycemic A normal value for the HgbA1c test is 6.0%–6.5%.14 levels in some patients.17,18,19 If a patient’s levels are greater than 7.9%, it is indicative of poor control and will require the intervention of the The following has also been confirmed:20 patient’s physician. Antibiotic prophylaxis will be neces- • The severity of periodontal disease increases with the sary for any emergency dental treatment in these poorly- duration of diabetes. controlled diabetic patients.12 • Periodontitis is an infection that is twice as prevalent in diabetic individuals as in nondiabetics. Periodontal Inflammation and • Severe periodontal infections are much more common Respiratory Disease in type II diabetics and can worsen the metabolic The oral cavity has long been considered a potential res- control of diabetes. ervoir for respiratory pathogens. Mechanisms of infection • The chronic nature of periodontal infection can be due to aspiration into the lungs of the oral pathogens represents a greater long-term risk for the diabetic capable of causing pneumonia. In hospitalized patients and acute infections. those in nursing homes, bacteria that colonize the teeth • P. gingivalis is able to sustain systemic inflammation, can potentially be aspirated into the lungs and can lead to which is another reason why diabetics need to have pneumonia and decreased overall lung function which is their chronic periodontitis treated. measured by spirometry.13

4 www.ineedce.com Effective plaque control must be monitored in at-risk patients. Power toothbrushes Five Steps to Bone Health* and/or use of an antimicrobial toothpaste 1. Take recommended daily amounts of vitamin D or rinse can be effective options. and calcium. 2. Engage in weight-bearing exercise. 3. Avoid smoking and excessive alcohol. 4. Consult a physician about bone health. There are two routes of spreading oral microorganisms 5. Have a bone density test and take medication to the lower respiratory tract: hematogenous (via blood when appropriate. pathway) and aspiration. The hematogenous route is rare. However, aspiration is much more common. Aspiration of *National Osteoporosis Foundation material from the upper airway occurred in 45% of healthy subjects and in 70% of subjects with impaired conscious- health professionals provide improved means to prevent, ness in one study. Periodontal disease and poor oral hygiene diagnose, and treat this disease.21 Osteoporosis tends to might result in a higher concentration of oral pathogens in take place in postmenopausal women not receiving hor- the saliva, sufficient in amount to overwhelms local im- mone treatment. Common signs of a person with osteopo- mune defenses. Dental plaque may also harbor colonies of rosis are petite stature and common fractures to long bones. pulmonary pathogens and promote their growth.13 The diagnosis of osteoporosis can be via radiographs, The symptoms of chronic obstructive pulmonary symptomology, and blood workup. A common treatment disease (COPD) and pneumonia are difficulty breathing, for osteoporosis is hormone replacement with estrogen.12 constant coughing up of phlegm, flu-like symptoms, and However, due to the onset of breast cancer, medications fatigue. If a patient presents with these symptoms, it is such as bisphosphonates (e.g. alendrolate—brand name necessary to refer the patient to his/her physician for fur- Fosamax®) are being used. These medications prevent the ther workup. action of osteoclasts. In addition, there is some evidence that some medications used to treat osteoporosis can be Periodontitis and Osteoporosis helpful in the management of periodontal disease.21,22 Osteoporosis is a debilitating metabolic bone disease that primarily affects elderly women. There is increasing Controlling Oral Inflammation evidence that osteoporosis and the underlying loss of bone Inflammation is a protective process to fight injury and in- mass is associated with periodontal disease and tooth loss. fection. While its purpose is to help in healing and removal Current evidence, including several prospective studies, of infection, its actions can be harmful. Therefore, it is im- supports an association of osteoporosis and the onset and portant that a patient maintain good oral hygiene. Dental progression of periodontal disease in humans.21 professionals realize that this is not an easy task for most Potential mechanisms by which host factors may in- patients to accomplish on their own. Compliance with oral fluence the onset and progression of periodontal disease, hygiene regimens can be time-consuming, and many pa- directly or indirectly, include underlying low bone density tients may lack the dexterity required to effectively remove in the oral cavity, bone loss as an inflammatory response plaque from all surfaces. to infection, genetic susceptibility, and shared exposure to In order to fight oral inflammation, mechanical removal risk factors.21 of pathogens via scaling and root planing in a diseased Some studies have suggested that hormone replace- sulcus/pocket is important. Therefore, a prophylaxis/ ment therapy is associated with retention of more teeth in periodontal maintenance schedule based on the patient’s old age. Nutritional factors also play a role in modifying needs (not insurance status) must be recommended. Lo- periodontal disease, such as vitamin D and calcium.22 Cal- cally-applied antimicrobials (LAA), such as PerioChip®, cium is used for building bones and teeth and in maintain- Arestin® and Atridox®, can be beneficial in periodontal ing bone strength. Vitamin D plays a major role in calcium pockets 5mm or more in depth. These products can release absorption. The relationship between calcium absorption medication into the periodontal pockets for a length of and vitamin D is similar to that of a locked door and a time, reducing the bacterial/inflammatory challenge and key. Vitamin D is the key that unlocks the door and allows creating an environment for better healing. calcium to leave the intestine and enter the bloodstream. To increase the effectiveness of patient home care, Vitamin D also works in the kidneys to help reabsorb cal- additional therapies are recommended. One option is the cium that otherwise would be excreted.24 inclusion of an antimicrobial/anti-inflammatory tooth- Systemic loss of bone density in osteoporosis, including paste that contains triclosan with a copolymer (Colgate® that of the oral cavity, may provide a host system that is Total®). Triclosan kills bacteria by interfering with the increasingly susceptible to infectious destruction of peri- enzyme necessary for fatty-acid synthesis.23 In addition, odontal tissue. Understanding this association will help triclosan works directly on the inflammation process by www.ineedce.com 5 directly inhibiting potent inflammatory mediators. Add- in periodontitis and cardiovascular disease.. Ann Periodontol. 2001:;6(1):30-40. ing an antimicrobial in this fashion offers benefit without 4. Beck J, Garcia R, Hass G, Vokonas P, Offenbacker S. Periodontal an additional step and therefore reduces compliance as an disease and cardivascular disease. J Periodontol. 1996;67:1123-37. issue. Another means of adding an antimicrobial is in the 5. Kuramitsu HK, Qi M, Kang I, Chen W. Role for periodontal form of a mouth rinse. bacteria in cardiovascular diseases. Ann Periodontol. 2001;6:41-7. 6. Kuramitsu H, Kang I, Qi M. Interactions of Porphyromonas Chlorhexidine gluconate is a broad-spectrum anti- gingivalis with host cells: implications for cardiovascular diseases. J septic antimicrobial. It can be used as a rinse to prevent Periodontol. 2003;74(12):85-9. gingivitis by reducing and inhibiting the formation of 7. Noack B, Genco RJ, Trevisan M, Grossi S, Zambon JJ, DeNardin plaque and as an LAA for the reduction of periodontal E. Periodontal infections contribute to elevated systemic C-reactive protein level. J Periodontol. 2001;72(9):1221-7. ® pockets (PerioChip ). Because it is positively charged, it 8. Mattilla et al. Association between dental health and acute binds to the oral mucosa and bacterial biofilm for up to 12 myocardial infarction. Br Med J. 1989;298:779-82. hours (and longer based on the delivery system). For this 9. DeStefano F, Anda R, Kahn H et al. Dental disease and risk of reason, chlorhexidine is a highly effective adjunct therapy. coronary artery disease and mortality. Br Med J. 1993;306:688-91. 10. Geerts SO, Nys M, de MP, Charpentier J, Alberts A, Legrand V, Another rinse option is stannous fluoride, which acts as an Rompen EH. Systemic release of endotoxins induced by gentle antibacterial and inhibits the formation of plaque. mastication: association with periodontitis severity. J Periodontol. If periodontal health cannot be obtained through 2002(73):73-8. regular periodontal maintenance and good oral hygiene, 11. Dorfer CE, Becher H, Ziegler CM, Kaiser C, Lutz R, Jorss D, Lichy C, Buggle F, Bultmann S, Preusch M, Grau AJ. The association of then the patient should be referred to a periodontist. A gingivitis and periodontitis with ischemic stroke. J Clin Periodontol. patient should also be referred if he/she has diabetes or 2004;31(5):396-401. cardiovascular disease along with periodontal disease for 12. Little J. Dental management of a medically compromised patient. management of periodontal inflammation. 6th edition. Elsevier Science Health Science div; 2002. 13. Mojon P. Oral health and respiratory disease. J Can Dent Assoc. 2002;68(6):340-5. Conclusion 14. Piche JE, Swan RH, Hallmon WW. The glycosylated hemoglobin Inflammation, although a protective process, can be assay for diabetes: its value to the periodontist.Two case reports. J harmful. Periodontitis is the result of inflammation to the Periodontol. 1989;60(11):640-2. 15. Mealey B. Periodontal implications: medically compromised periodontium, and cytokines, or chemical mediators, are patients. Ann Periodontol. 1996:256-269. the result of inflammatory cells fighting against bacterial 16. Ryan ME, Carnu O, Kamer A. The influence of diabetes on the plaque. High amounts of these mediators can affect the periodontal tissues. J Am Dent Assoc.2003;134:34S-40S. body’s systems, especially the arteries, and can potentially 17. Taylor GW. Bidirectional interrelationships between diabetes and periodontal diseases: an epidemiologic perspective. Ann cause more harm in a patient with compromised cardio- Periodontol 2001;6:99-110. vascular health. Dental professionals should include blood 18. Soskolne WA, Klinger A. The relationship between periodontal pressure screenings as part of their patient assessment diseases and diabetes: an overview. Ann Periodontol. 2001;6:91-9. practices and discuss heart-healthy strategies. 19. Iacopino A. Periodontitis and diabetes interrelationships: role of inflammation. J Periodontol. 2001;6:125-37. Dental professionals should assess risk for patients 20. Grossi S. Treatment of periodontal disease and control of diabetes: with diagnosed (or undiagnosed) diseases such as diabetes, an assessment of the evidence and need for future research. Ann respiratory diseases, and osteoporosis, and refer patients to Periodontol. 2001; 6(1):138-45. a physician or periodontist as necessary. 21. Wactawski-Wende J. Periodontal diseases and osteoporosis: association and mechanisms. Ann Periodontol. 2001;6:197-208. It is very important to evaluate and monitor oral hy- 22. Krall EA. The periodontal-systemic connection: implications for giene in at-risk patients. The inclusion of antimicrobials treatment of patients with Osteoporosis and Periodontal Disease. as a part of patient home care to enhance plaque control Ann Periodontol. 2001;1(6):209-13. should also be considered. 23. Cullinan MP, Westernman B, Hamlet SM, Palmer JE, Faddy MJ, Seymour GJ. The effect of triclosan-containing dentifrice on progression of periodontal disease in an adult population. J Clin Registered Trademarks Periodontol. 2003;30(5):414-9. Fosamax® (MERCK & CO, INC., Whitehouse Station, NJ) 24. National Osteoporosis Foundation. Available at www.nof.org/ PerioChip® (OMNII Oral Pharmaceuticals, West Palm Beach, FL) prevention/calcium.htm. Arestin® (OraPharma, Warminster, PA) Atridox® (CollaGenex Pharmaceuticals, Newtown, PA) Colgate® Total® (Colgate Palmolive, New York, NY) Author Profiles

References Richard Nejat, DDS 1. Ramzi S, Contran, SL, Robbins V, Kumar V, Robbins J, Perkins. Dr. Richard Nejat received his Doctor- Basic Pathology 7th edition. Harcourt Publishers LTD; 2002. ate of Dental Surgery from New York 2. Fleming T. Periodontitis. Ann Periodontol. 1999 International work-shop for classification of periodontal diseases and conditions. University, where he graduated in the 1999;4:32-5. top of his class, receiving the prestigious 3. De Nardin E. Role of Inflammatory and immunological mediators OKU honors. Following graduation, Dr.

6 www.ineedce.com Nejat began a three-year residency in periodontics and dental from the University of Medicine and implants at Stony Brook University-State University of New Dentistry of New Jersey, New Jersey York, where he earned his certificate in periodontics. He is Medical School. His internship and resi- an active instructor in professional continuing education on dency in pediatrics were completed at topics including periodontal medicine, computer-guided and North Shore University Hospital, Cor- minimally invasive dental implant surgery, and periodontal nell University Medical College. His plastic surgery. allergy/immunology fellowship was performed at the R.A. Dr. Nejat is currently involved in numerous clinical Cooke Institute of Allergy at St. Luke’s/Roosevelt Hos- research projects involving flapless dental implant sur- pital Center, Columbia University College of Physicians gery, minimally invasive periodontal plastic surgeries, and and Surgeons. Dr. Nejat is Board Certified in pediatrics computer-guided dental implant surgery with immediate and has received appointments in pediatrics at St. Luke’s/ function. Dr. Nejat is a Diplomate of the American Board of Roosevelt Hospital Center and Bellevue Hospital Center Periodontology. He maintains private practices in Manhat- in New York City. tan, NY and Nutley, NJ. Dr. Nejat is frequently quoted in the media, including NBC news, Fox News, WB11 News, ABC news and Daniel Nejat, DMD numerous consumer publications. He also frequently lec- Dr. Daniel Nejat graduated magna cum tures to physicians and consumers on the topics of allergy, laude from Drew University with a Bach- asthma, eczema and food allergies. elor of Arts. He continued his education by receiving a Doctorate in Dental Medi- Disclaimer cine at the University of Medicine and The authors of this course have no commercial ties with the Dentistry of New Jersey Dental School. Presently, Dr. Nejat sponsors or the providers of the unrestricted educational is completing his postdoctoral periodontal residency at the grant for this course. New York University College of Dentistry. Reader Feedback Morris Nejat, MD We encourage your comments on this or any PennWell course. Dr. Morris Nejat graduated cum laude from Drew Uni- For your convenience, an online feedback form is available at versity in New Jersey and obtained his medical degree www.ineedce.com.

www.ineedce.com 7 Questions

1. Inflammation represents the 12. Research has shown that: 21. Diabetes mellitus type I is caused by body’s protective response against a. Patients with a history of MI typically have ______, while type II is a result of ______. good oral health. ______due to tissue resistance. a. injury and tissue modification b. The incidence of mortality and a. impaired insulin action; defective secretion of b. injury and tissue destruction CHD increases with the severity of insulin b. impaired insulin action; overactive secretion of c. salivary antagonism periodontal disease. d. all of the above insulin c. A 20% increase in periodontal bone loss has no c. defective secretion of insulin; impaired insulin 2. Which of the following statements effect on CHD. action are true? d. Both b and c. d. none of the above a. Inflammation consists of coordinated events at both the cellular and tissue level. 13. Cellular mediator TNF-α is found 22. Antibiotic prophylaxis is ______b. Inflammation can destroy an injurious agent in chronic periodontitis and is as- for any emergency dental treatment (e.g. bacteria). sociated with lowering “good lipids” in poorly-controlled diabetic c. Inflammation can be harmful to the host. known as: patients. d. all of the above. a. LDL a. not necessary b. PDL b. occasionally necessary 3. Clinical signs of periodontal inflam- c. often necessary c. HDL d. necessary mation do NOT include: d. MOL a. Redness and heat. 23. The oral cavity is a potential b. Edema and pain. 14. Periodontal pockets are a chronic reservoir for ______pathogens. c. Headaches. source of passage of ______into a. respiratory d. Swelling and loss of function. the bloodstream. b. renal 4. Tissue damage in periodontal disease a. anti-inflammatory bacterial components c. urinary is the result of inflammatory compo- b. anti-inflammatory viral components d. brachial nents activated by the ______. c. pro-inflammatory bacterial components 24. Bacteria that colonize the teeth can a. bacterial response d. pro-inflammatory viral components ______. b. viral response 15. Diabetes is: a. be aspirated into the lungs c. host response b. lead to pneumonia d. cytokine response a. Not very common. c. decrease overall lung function b. A chronic metabolic disorder. d. all of the above 5. Inflammation occurs when the body c. Controllable to prevent complications. detects ______from host cells. d. b and c. 25. Oral microorganisms spread to the a. exotoxins lower respiratory tract through: b. mesotoxins 16. Patients with uncontrolled diabe- a. A hematogenous route (via blood pathway). c. endotoxins tes are prone to oral complications b. Aspiration. d. chemotoxins such as: c. Osmosis. d. a and b. 6. Cell mediators are messenger cells a. Gingivitis and periodontal disease. that ______the area of infection. b. Fungal infections. 26. There is increasing evidence that a. relay other cells into c. Caries due to xerostomia. ______and the underlying loss b. reduce other cells in d. All of the above. of bone mass are associated with periodontal disease and tooth loss. c. release other cells on 17. There is a bidirectional relationship d. recruit other cells into a. osteoblastomas between periodontal disease and b. osteogenesis 7. The chemical mediator IL-1 recruits diabetes that indicates that the c. osteoporosis osteoclasts, which are bone-building severity of: d. osteoplasty cells. a. Diabetes will increase as periodontal disease 27. There is some evidence that some a. osteoblasts gets worse. medications used to treat ______b. osteoclasts b. Periodontal disease will increase as control of can be helpful in management of c. fibroblasts diabetes worsens. periodontal disease. d. fibroclasts c. a and b. a. Parkinson’s disease 8. The presence of ______levels of d. None of the above. b. osteoporosis chemical mediators can be harmful. c. Crohn’s disease 18. The severity of periodontal disease d. none of the above a. lowered ______with the duration of b. nonexistent diabetes. 28. Antimicrobials that are effective in c. elevated the inhibition of plaque are: d. none of the above a. decreases b. remains the same a. Triclosan. 9. Atherosclerosis is the thickening and c. increases b. Chlorhexidine. c. Stannous fluoride. hardening of the: d. a or b d. All of the above. a. PDL. b. Blood-brain barrier. 19. Clinical manifestations of 29. Triclosan is effective because it: c. Arteries. poorly-controlled or uncontrolled a. Kills bacteria by interfering with the enzyme d. Intestinal lining. diabetics are: necessary for fatty-acid synthesis. a. Burning mouth or tongue. b. Directly inhibits potent inflamma- 10. ______are chronic inflamma- b. Polydipsia (increased thirst). tory mediators. tory diseases. c. Altered taste sensation. c. Is an antiseptic, and bacteria will not develop a. Atherosclerosis and Parkinson’s disease d. All of the above. resistance to it. b. Parkinson’s disease and periodontitis d. All of the above. c. Atherosclerosis and periodontitis 20. Periodontitis is an infection that d. none of the above 30. The inclusion of antimicrobials into is ______prevalent in diabetic the oral hygiene process can help 11. CRP is found in ______. individuals as in nondiabetics. ______plaque control. a. periodontitis a. not as a. reduce b. cardiovascular disease b. as b. maintain c. response to infection c. more c. enhance d. all of the above d. none of the above d. none of the above

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Requirements for successful completion of the course and to obtain dental continuing education credits: 1) Read the entire course. 2) Complete all information above. 3) Complete answer sheets in either pen or pencil. 4) Mark only one answer for each question. 5) A score of 70% on this test will earn you 2 CE credits. 6) Complete the Course Evaluation below. 7) Make check payable to PennWell Corp.

Mail completed answer sheet to Educational Objectives Academy of Dental Therapeutics and Stomatology, 1. List and describe the mechanism by which periodontal disease causes production of inflammatory mediators that enter A Division of PennWell Corp. the systemic circulation and affect organ systems in the body P.O. Box 116, Chesterland, OH 44026 2. List and describe the mechanism by which inflammatory mediators effect vessel plaque formation and lead to an or fax to: (440) 845-3447 increased risk of cardiovascular disease 3. List and describe the mechanism by which periodontal disease mediators worsen the condition in diabetes mellitus For immediate results, go to www.ineedce.com 4. Describe the association of periodontal disease and the increased risk of development of pneumonia and COPD in and click on the button “Take Tests Online.” Answer the elderly sheets can be faxed with credit card payment to (440) 845-3447, (216) 398-7922, or (216) 255-6619. 5. Describe the probable association of periodontal disease, tooth loss, and osteoporosis Payment of $49.00 is enclosed. 6. Describe how appropriate treatment of periodontal disease can lead to improvement in outcomes in many of the above (Checks and credit cards are accepted.) disease processes. If paying by credit card, please complete the following: MC Visa AmEx Discover Acct. Number: ______Course Evaluation Please evaluate this course by responding to the following statements, using a scale of Excellent = 5 to Poor = 0. Exp. Date: ______Charges on your statement will show up as PennWell 1. Were the individual course objectives met? Objective #1: Yes No Objective #4: Yes No Objective #2: Yes No Objective #5: Yes No Objective #3: Yes No Objective #6: Yes No 2. To what extent were the course objectives accomplished overall? 5 4 3 2 1 0 3. Please rate your personal mastery of the course objectives. 5 4 3 2 1 0 4. How would you rate the objectives and educational methods? 5 4 3 2 1 0 5. How do you rate the author’s grasp of the topic? 5 4 3 2 1 0 6. Please rate the instructor’s effectiveness. 5 4 3 2 1 0 7. Was the overall administration of the course effective? 5 4 3 2 1 0 8. Do you feel that the references were adequate? Yes No 9. Would you participate in a similar program on a different topic? Yes No 10. If any of the continuing education questions were unclear or ambiguous, please list them. ______11. Was there any subject matter you found confusing? Please describe. ______12. What additional continuing dental education topics would you like to see? ______AGD Code 490

PLEASE PHOTOCOPY ANSWER SHEET FOR ADDITIONAL PARTICIPANTS.

AUTHOR DISCLAIMER INSTRUCTIONS COURSE CREDITS/COST RECORD KEEPING The authors of this course have no commercial ties with the sponsors or the providers of All questions should have only one answer. Grading of this examination is done All participants scoring at least 70% (answering 21 or more questions correctly) on the PennWell maintains records of your successful completion of any exam. Please contact our the unrestricted educational grant for this course. manually. Participants will receive confirmation of passing by receipt of a verification examination will receive a verification form verifying 2 CE credits. The formal continuing offices for a copy of your continuing education credits report. This report, which will list form. Verification forms will be mailed within two weeks after taking an examination. education program of this sponsor is accepted by the AGD for Fellowship/Mastership all credits earned to date, will be generated and mailed to you within five business days SPONSOR/PROVIDER credit. Please contact PennWell for current term of acceptance. Participants are urged to of receipt. This course was made possible through an unrestricted educational grant. No EDUCATIONAL DISCLAIMER contact their state dental boards for continuing education requirements. PennWell is a manufacturer or third party has had any input into the development of course content. The opinions of efficacy or perceived value of any products or companies mentioned California Provider. The California Provider number is 4527. The cost for courses ranges CANCELLATION/REFUND POLICY All content has been derived from references listed, and or the opinions of clinicians. in this course and expressed herein are those of the author(s) of the course and do not from $49.00 to $110.00. Any participant who is not 100% satisfied with this course can request a full refund by Please direct all questions pertaining to PennWell or the administration of this course to necessarily reflect those of PennWell. contacting PennWell in writing. Machele Galloway, 1421 S. Sheridan Rd., Tulsa, OK 74112 or [email protected]. Many PennWell self-study courses have been approved by the Dental Assisting National Completing a single continuing education course does not provide enough information Board, Inc. (DANB) and can be used by dental assistants who are DANB Certified to meet © 2008 by the Academy of Dental Therapeutics and Stomatology, a division COURSE EVALUATION and PARTICIPANT FEEDBACK to give the participant the feeling that s/he is an expert in the field related to the course DANB’s annual continuing education requirements. To find out if this course or any other of PennWell We encourage participant feedback pertaining to all courses. Please be sure to complete the topic. It is a combination of many educational courses and clinical experience that PennWell course has been approved by DANB, please contact DANB’s Recertification survey included with the course. Please e-mail all questions to: [email protected]. allows the participant to develop skills and expertise. Department at 1-800-FOR-DANB, ext. 445.